When You Swallow A Grenade

In 1941, a rose killed a policeman.

Albert Alexander, a 43-year-old policeman in Oxford, England, was pruning his roses one fall day when a thorn scratched him at the corner of his mouth. The slight crevice it opened allowed harmless skin bacteria to slip into his body. At first, the scratch grew pink and tender. Over the course of several weeks, it slowly swelled. The bacteria turned from harmless to vicious, proliferating through his flesh. Alexander eventually had to be admitted to Radcliffe Hospital, the bacteria spreading across his face and into his lungs.

Alexander’s doctors tried treating him with sulfa drugs, the only treatment available at the time. The medicine failed, and as the infection worsened, they had to cut out one of his eyes. The bacteria started to infiltrate his bones. Death seemed inevitable.

But then, on February 12, 1941, Alexander was injected with an experimental drug: a molecule produced by mold.

The molecule was, of course, penicillin. It had been discovered thirteen years earlier but soon abandoned because there didn’t seem to be any way to turn it into an effective drug. In the late 1930s, Howard Florey and his colleagues at the University of Oxford revived the drug and began testing it on mice. They found the penicillin could cure them of infections by killing their bacteria. Florey then gave a dose of penicillin to a woman dying of cancer and found that it wasn’t toxic to her.

Now Florey and his colleagues wanted to see if it could stop an infection in a human being. Alexander, with nothing left between him and death, was their first subject.

“Striking improvement” was how Florey described what happened next. Within a day, Alexander’s infections were subsiding. After a few more days, his fever broke and much of his face cleared up.

An early apparatus for collecting penicillin

Florey could have saved Alexander’s life, if he hadn’t run out of penicillin after a few days. Nobody but Florey knew how to make the stuff, and his recipe only yielded a tiny amount at a time. To stretch out their supply of penicillin, a member of Florey’s lab would visit the hospital each morning to collect Alexander’s urine. He would carry it back by bicycle to the lab, where the scientists extracted the penicillin that Alexander’s body hadn’t absorbed. Alexander’s doctors then injected the recycled antibotic into Alexander’s arm.

But the salvaging operation didn’t recover enough penicillin to keep the bacteria from growing again. The infection returned and grew worse than before. On March 15, Alexander died. In his final report, Florey called Alexander’s death “a forlorn case.”

It is hard to imagine a time when a scratch could so easily lead to death. Albert Alexander died precisely at the dawn of the Antibiotic Era. Shortly after failing to save Alexander’s life, Florey harvested more penicillin and gave it to another patient at the hospital, a 15-year-old boy who had developed an infection during surgery. They cured him in a few days. Within three years of Alexander’s death, Pfizer was manufacturing penicillin on an industrial scale, packing 7500-gallon tanks with mold, fed on corn steep liquor. In that same year, Selman Waksman, a Rutgers microbiologist, and his colleagues discovered antibiotics made by soil bacteria, such as streptomycin and neomycin.

What made antibiotics so wildly successful was the way they attacked bacteria while sparing us. Penicillin, for example, stops many types of bacteria from building their cell walls. Our own cells are built in a fundamentally different way, and so the drug has no effect. While antibiotics can discriminate between us and them, however, they can’t discriminate between them and them–between the bacteria that are making us sick and then ones we carry when we’re healthy. When we take a pill of vancomycin, it’s like swallowing a grenade. It may kill our enemy, but it kills a lot of bystanders, too.

It’s understandable that few scientists gave this fact much thought in the 1940s, when the lives of people like Albert Alexander hung in the balance. Even if they did wonder about the 100 trillion microbes that live in our healthy bodies–known as the microbiome–they were poorly equipped to investigate them. They could only study bacteria that they could rear in their labs. E. coli thrived outside of the body, sucking in oxygen and feeding on just about any sugar on offer. That’s why scientists now understand E. coli better than any other species on Earth.

But in its natural habitat–the human gut– E. coli is a rare bird. Only about one microbe in a thousand in the gut belongs to the species. The rest of the microbes are far too fussy to survive in just any Petri dish. They need a special balance of gases, acidity, and nutrients. In many cases, they can’t survive unless they’re living alongside other species. Their fussiness has slowed down scientists trying to explore the microbiome. But now that they can fish out the DNA of the microbiome, scientists are beginning to get a sense of the staggering diversity of microbes we harbor.

Each of us is home to several thousand species. (I’m only talking about bacteria, by the way–viruses, fungi, and protozoans stack an even higher level of diversity on top of the bacterial biodiversity.) My own belly button, I’ve been reliably informed, contains at least 53 species. Many of the species I harbor are different than the ones you harbor. But if you look at the kinds of genes carried by those species, our microbiomes look very similar. That’s partly because surviving on a human body requires certain skills, so any species that is going to last long in your lungs, say, will need many of the same genes.

Three vital organs

But the similarity speaks to something else. The microbiome keeps us healthy. It breaks down some of our food into digestible molecules, it detoxifies poisons, it serves as a shield on our skin and internal linings to keep out pathogens, and it nurtures our immune systems, instructing them in the proper balance between vigilance and tolerance. It’s a dependence we’ve been evolving for 700 million years, ever since our early animal ancestors evolved bodies that bacteria could colonize. (Even jellyfish and spongeshave microbiomes.) If you think of the human genome as all the genes it takes to run a human body, the 20,000 protein-coding genes found in our own DNA are not enough. We are a superorganism that deploys as many as 20 million genes.

It’s not easy to track what happens to this complex organ of ours when we take antibiotics. Monitoring the microbiome of a single person demands a lot of medical, microbiological, and genomic expertise. And it’s hard to generalize, since each case has its own quirks. What happens to the microbiome depends on the particular kind of bacteria infecting people, the kind of antibiotics people take, the state of their microbiome beforehand, their own health, and even their own genes (well, the human genes, at least). And then there’s the question of how long these effects last. If there’s a change to the microbiome for a few weeks, does that change vanish within a few months? Or are there effects only emerge years later?

Scientists are only now beginning to get answers to those questions. In a paper just published online in the journal Gut, Andres Moya of the University of Valencia and his colleagues took an unprecedented look at a microbiome weathering a storm of antibiotics. The microbiome belonged to a 68-year-old man who had developed an infection in his pacemaker. A two-week course of antbiotics cleared it up nicely. Over the course of his treatment, Moya and his colleagues collected stool samples from the man every few days, and then six weeks afterwards. They identified the species in the stool, as well as the genes that the bacteria switched on and off.

What’s most striking about Moya’s study is how the entire microbiome responded to the antibiotics as if it was under a biochemical mortar attack. The bacteria started producing defenses to keep the deadly molecules from getting inside them. To get rid of the drugs that did get inside them, they produced pumps to blast them back out. Meanwhile, the entire microbiome powered down its metabolism. This is probably a good strategy for enduring antibiotics, which typically attack the molecules that bacteria use to grow. As the bacteria shut down, they had a direct effect on their host: they stopped making vitamins and carrying out other metabolic tasks.

In another intriguing response, the microbes dimmed their immune systems. To defend against invading viruses, bacteria deploy a collection of enzymes that recognize foreign genes and chop them up. As the bacteria dialed these enzymes down, they may have allowed viruses to infect them more easily. In some cases, the invasion led to their death. But in other cases, the viruses may have delivered them useful genes, including genes that let them resist the antibiotics.

Moya and his colleagues found that some types of bacteria were able to survive the onslaught of antibiotics, while others failed. As a result, the overall diversity of bacteria in the man’s gut changed from day to day over the course of his treatment. Before he started taking antibiotics, the scientists identified 41 species in a stool sample. By day 11, they only found 13. Six weeks after the antibiotics, the man was back up to 38 species. But the species he carried six weeks after the antibiotics did not represent that same kind of diversity he had before he took them. A number of major groups of bacteria were still missing.

This long-term disturbance was not unusual. Other scientists have tracked the diversity of the microbiome for many months after people get antibiotics. Even after all that time, the microbiome may not return to its original state. By disturbing our inner ecosystem, antibiotics can affect our own health.

In some cases, for example, antibiotics can make it easier for pathogens to invade. Eric Pamer of Memorial Sloan Kettering Cancer Center and his collegues recently provided a striking demonstration of this effect. They gave mice a single dose of the antibiotic clindamycin. Ninety percent of the diversity in the gut of the mice disappeared and was still gone four weeks after the treatment. The scientists then inoculated the mice with the spores of Clostridium difficile, a particularly nasty pathogen that can cause lethal cases of diarrhea. They invariably got an overwhelming infection, and half of them died within a few days. Pamer could wait as long as ten days after giving the mice antibiotics, and they were still felled by C. difficile. Healthy mice, on the other hand, easily kept the invasion in check.

Antibiotics may also exert subtler, longer-term effects on our health. Matthew Kronman of Seattle Children’s Hospital and his colleagues, for example, recently reviewed the medical records of over a million people. They found that children who took antibiotics were at greater risk of developing inflammatory bowel disease later in life. The more antibiotics they took, the greater the risk. Similar studies have found a potential link to asthma as well.

A study carried out by Dennis Kasper at Harvard hints at how antibiotics can send the immune system off the rails. They reared mice in isolated containers so that they never developed a microbiome. The germ-free rodents developed unusually high levels of an aggressive type of immune cell called an invariant natural killer T cell. If Kasper inoculated baby germ-free mice with a normal microbiome, the T cells remained rare. Antibiotics, the scientists propose, allow the T cells to explode and to run amok.

It’s even possible that long-term antibiotic use may influence how people put on fat. Martin Blaser of New York University and his colleagues carried out an experiment on mice in which they fed the animals antibiotics and then tracked their metabolism. The scientists found that the mice fed with antibiotics developed a higher percentage of body fat than mice that didn’t.*

Antibiotics cause this rise in fat, Blaser and his colleagues argue, by creating long-term changes in the microbiome. The species fostered in the mice produce enzymes that change not just how they break down our food, but also send signals to our own hormones to change the way we store energy from our food.

None of these results would ever lead a doctor to give up on antibiotics altogether. Seventy years after Albert Alexander died, they remain the best tool we have to fight off deadly infections. But we shouldn’t be blasé about them. Doctors often prescribe antibiotics to patients simply on the hunch that they have a bacterial infection. It often turns out that viruses are causing the trouble instead. Many parents are all too familiar with the endless cycle of ear infections and antibiotics. That cycle may take a toll.

There are changes that would help fight against that toll–some that we could make right away, and others that will demand a lot more research before becoming practical. We could become less casual about asking doctors for antibiotics. If DNA-sequencing becomes cheap enough, doctors might become able to diagnose bacteria infections quickly and accurately, so as not to prescribe antibiotics when they can’t help. And when it turns out we are infected, there are other ways to fight bacteria. For a century, some scientists have explored using bacteria-infecting viruses as a weapon against infections, for example.

It might even be possible to fight bacteria with bacteria. Instead of blasting both pathogens and harmless microbes alike, we might tend the microbial garden better and keep down the weeds. The most dramatic example of this gardening is the fecal transplant. Half a million people get C. difficile infections a year, many of which can’t be stopped by antibiotics. Doctors have found that a little stool from a healthy donor can crush these invasions. Fecal transplants may also help against inflammatory bowel disease, by restoring the immune system’s essential partners. Transplants might treat infections elsewhere in the body, from cavities in the mouth to rashes on the skin.

These treatments would do more than tamp down the harmful effects of antibiotics. They’d also help keep antibiotics themselves useful. When Florey first tried out penicillin against Alexander and other patients, he worried that the bacteria might adapt to the drug. It eventually did; for many pathogens, penicillin is now useless because they’ve evolved strong resistance against it. C. difficile and many other pathogens have become resistant against many other antibiotics, too. Developing new antibiotics is essential for stopping this decline, but we will need to use them just as sparingly to slow down evolution’s relentless push.

Otherwise, we may return to a time when roses killed policemen.

[This post emerged from the research I did for a talk I gave last week at Rutgers]

[Images: Grenade, Wikipedia; thorn, macrophile on Flickr via Creative Commons; bacteria, Health Research Board on Flickr via Creative Commons; Penicillin, NIH ]

[Update 12/18 11 am: Fixed Howard Florey’s name.]

[*Upate 12/20 7:20 am: In the original version, I incorrectly stated that the mice’s overall body mass increased. This was only true among female juveniles. By seven weeks, however, there was no increase in body mass–only its composition of fat and lean mass. Thanks to zmil for pointing out my error.]

65 thoughts on “When You Swallow A Grenade

  1. Howard Walter Florey, one of the guys who won a nobel for the discovery of Penicillin, was an Australian (and is celebrated as a famous Nobel prize winning scientist 🙂

  2. Psst, you missed a word: “Antibiotics may subtler, longer-term effects”
    Otherwise, interesting article as always 🙂

    [CZ: Thanks! Fixed.]

  3. This is an interesting article, but there are too many proofreading errors, in particular paragraphs 4, 16, and 21.

    [CZ: I do the best I can, Robert. Corrections are always appreciated.]

  4. This article leads me to question the practice of the “Big Meat” industry to routinely inject cattle with antibiotics. Perhaps there is a direct correlation to the rapidly increasing rates of childhood obesity and other ilnesses that have emerged.

    [CZ: I’m not aware of any research showing antibiotics given to livestock can survive all the way to the dinner table. It seems highly unlikely based on basic physiology. The real worry about antibiotics on farms is the immense amount of research indicating that they select for resistant bacteria, which can then leave the farm and make us sick and defy medical treatment.]

  5. In cases OTHER THAN bowel infections, why not store a stool sample from the patient before antibiotics are started, then give the patient an autologous stool transplant from that sample once the course of antibiotics is completed?

  6. I believe that Selman Waksman did not discover streptomycin although he certainly took credit for it. According to a book I read last year his research student, Albert Schatz, working under dangerous conditions in a basement lab (Waksman would not even enter the lab in which this work was done) worked day and night to accomplish this task. Waksman did not disclose to his student the fact that he was personally receiving funds from a drug manufacturer and took public credit for work he did not even supervise. I cannot recall the name of this book but can find it if there is interest.

    [CZ: It’s called Experiment Eleven, by Peter Pringle. Here’s a piece by Pringle in the Times earlier this year.]

  7. Congratulations on an exceptional and thought-provoking blog. Love how you artfully tied the introduction to the conclusion–roses killing policeman. I didn’t realize that some of the good bacteria in our guts never grow back as a result of antibiotic use. Also, congrats on your new gig with National Geographic.

  8. Very good article Carl. Congratulations on your new “symbiosis” with National Geographic.

    “The most dramatic example of this gardening is the fecal transplant. Half a million people get C. difficile infections a year, many of which can’t be stopped by antibiotics. Doctors have found that a little stool from a healthy donor can crush these invasions.”

    Something similar is a common practice in Veterinary Medicine. When a ruminant, lets say a cow, has been treated with antibiotics and the number or activity of ruminal bioma is reduced, direct administration into the rumen cavity with the aid of a pipe of 6 liters of ruminal fluid from a healthy cow will be one of the best treatments.

    See Ruminal Fluid Transfer in http://www.merckmanuals.com/vet/pharmacology/systemic_pharmacotherapeutics_of_the_digestive_system/drugs_for_specific_purposes_in_the_ruminant_digestive_system.html?qt=administration%20of%20ruminal%20fluid&alt=sh#v3330567

    Best regards,


  9. Incredibly interesting article. I’m a retired microbiologist and never had a class discussing this particular topic. Thoroughly enjoyed it.

  10. The power of GMO is not only in the food, but in drugs and animals… Thanks god we got molecular biology to understand and modify the habitat in our benefit

  11. With the advent of ABs modern medicine turned its back on thousands of years of knowledge, and in particular, the applicability of many medicinal plants in bacterial infection. Some plants have as potent effects as the strongest ABs but without the same adverse effects. The reason for their efficacy is that they exert their antimicrobial activity through a variety of molecular mechanisms – not the “magic bullet” of using a single antibiotic – and thus don’t allow the organism to develop resistance so easily. Attached is a paper looking at Hydrastis canadensis (goldenseal) and its effects on MRSA. I have also attached a landmark study that demonstrated the synergy of an otherwise benign naturally occurring chemical called 5′-methoxyhydnocarpin and how it potentiates the activity of antibacterial alkaloids such as berberine. In addition, I would like to point out that ecological therapies already exist in the form of probiotic foods, e.g. sauerkraut, brine pickles, etc., and these can be highly effective ways to restore the human biome. This stuff isn’t theoretical, because I use such strategies every day in my practice.

    Quorum quenching and antimicrobial activity of goldenseal (Hydrastis canadensis) against methicillin-resistant Staphylococcus aureus (MRSA): http://www.ncbi.nlm.nih.gov/pubmed/22814821
    Synergy in a medicinal plant: antimicrobial action of berberine potentiated by 5′-methoxyhydnocarpin, a multidrug pump inhibitor: http://www.ncbi.nlm.nih.gov/pubmed/10677479

  12. @Brad Dawkins: Many of these critters don’t “store” well. Freezing (which would include freeze-drying) would markedly diminish the floral diversity in any samples stored for autologous donation. This isn’t to say it wouldn’t work- perhaps one or more of the critters useful for this sort of thing *do* survive freezing, but it remains conjecture. In the interim, folks are working on standardized solutions- stuff that would pass muster from a pharma standpoint- and provide a more hygienically-acceptable solution that could be generated in the lab with virtually no risk of pathogens (hepatitis, etc.), parasites, etc., and be more “palatable” from a patient’s perspective.

    And, of course, the ability to pad the company’s bottom line with a $12,000 solution instead of poop + installation fees.

  13. “The scientists found that the mice fed with antibiotics got bigger, and that extra weight was due to putting on extra fat.”

    A common misreading of the paper, unfortunately. The mice did not gain weight. Their fat percentage increased significantly, however. It’s an interesting result, but also quite confusing, as it doesn’t quite fit with previous studies where antibiotics actually caused weight gain.

    [CZ: Thanks. In retrospect, I realize that I was led astray by some of the findings from a “larger, confirmatory experiment” also described in the paper. It shows an increase in body mass in juvenile females, but no difference at seven weeks. I’ve fixed the text.]

  14. Another terrific post, Carl. With you, Ed Yong and Brian Switek in one place NG have really done well.

    One whinge – why is the space for comments so microscopic? (At least on my browser)

  15. When I use antibiotics, I always use yogurt pills or other probiotics to replenish the good bacteria.
    Not sure how much it helps though.

  16. Another excellent piece, Carl. I’ll have to get used to seeing your column here at Nat Geo from now on.

    I have a question: You give a great rundown of the pros and cons of antibiotics, the cons namely being collateral damage to our microbiome. With enough bacteria species sequenced, might we one day be able to synthesize antibiotics which target specific bacteria strains, and possibly even the specific disease-causing genes of those strains? By culling specific genes and shutting them down, could we thereby reduce or eliminate collateral damage to the benign microbes?

    Are these real or remote possibilities (discounting long-term success as the bacteria inevitably evolves their way around them)?

    [CZ: It is theoretically possible to do that. You could imagine RNAi, for example, that would only grab onto RNA produced by one strain of bacteria, and kill it. But for now that lies off in our sci-fi future, where people could tailor medicine to individual strains.]

  17. Carl, you mention the enormous quantities of ABs given to livestock. My impression is that they are so beloved by that industry because they cause the animals to gain weight quickly–not because they keep cows, pigs and chickens healthy. Perhaps the weight gain is disproportionately fat, and perhaps the presence of the drugs in the animals’ guts is detrimental to their overall health. Whether it makes their flesh less desirable as food, I don’t know.

    [CZ: In his new paper, Blaser does mention the possibility that the experiment could explain the changes seen in livestock put on antibiotics.]

  18. This article reminded me of the work of Eric Alm, where he tracked two microbiomes (his and a student’s) for a year, with interesting results:

  19. “Doctors often prescribe antibiotics to patients simply on the hunch that they have a bacterial infection. It often turns out that viruses are causing the trouble instead.”

    If that’s not a subtle damnation of the practice of medicine I don’t know what is. That someone–a doctor–would inoculate a subject with a potentially dangerous species or its toxin without first identifying the exact species they are trying to rid the body of first is anti-science. I’d say medieval, but at least they know microbes exist.

    Wondering if you’re involved with cleaning up the medical or health insurance industries like your fellow science writer G. Taubes. Best wishes… – lc

  20. Since my husband, who has Crohn’s Disease, just finished a round of antibiotics, I’m particularly interested in this topic. He’s controlled his symptoms with luck for 7 years and through diet for 2 years, and we’ve seen some impressive results with a powerful probiotic this fall when some minor symptoms returned.

    Our plan for taking his microbiome into our own hands after this round of abx is to make sure he takes the probiotic very regularly for at least 2 months. Are there any studies you’re aware of looking at the effect of probiotics on the replenishing of the microbiome after antibiotics? I always tell people that the gut (really the whole human person) after antibiotics is a bit like a newly tilled garden – fertile soil empty and waiting for whatever comes along. Leave it to its own devices, particularly with sugars in the diet, and the “weeds” will likely take root. It’s up to us to “sow” good bacteria by consuming probiotics. Does this philosophy make good medical sense?

    Thank you for the round up of research! I’ve been waiting for some of this data to keep in my virtual tool belt…

    Katie Kimball

    [CZ: I am not a doctor and do not offer medical advice. You should consult a doctor for that. Be aware that products sold as probiotics typically make claims that have not been evaluated by the FDA for safety or efficacy. Some probiotics show some promise, but many are probably useless. Once they get into the gut, they get outcompeted and become extinct. Anecdotes about a few people’s symptoms easing after taking probiotics are not enough data to have confidence in them. Here is an open-access review of the use of probiotics for Crohn’s disease and related bowel disorders.]

  21. Carl,
    Thanks so much for that journal article link. I know you have to include that disclaimer, but rest assured I’m not looking for medical advice- just a professional’s critique of whether my novice analogy is an accurate description of the effects of antibiotics on the body and the possibility of secondary infection afterward.

    I’d be curious to see a study on the effect of regular consumption of fermented foods as the source of probiotics, since traditionally, people have consumed fermented foods at each meal to promote digestive health.

    Thanks again for your insight!

  22. Mr. Zimmer,

    Our family frequently uses oil of oregano to treat colds and the flu. I have heard that oregano oil “kills” viruses by interrupting the virus communication, effectively preventing it from multiplying. However, I’ve always been curious about oregano’s effect on the good bacteria. Can you comment on that?

    Many thanks!

    [CZ: I first need to address your claim about oregano being effective against the flu and colds. There are no studies on humans that support these claims that I can find. There are a few studies that find some anti-viral activity of oregano in cell cultures, but that’s a long stretch (such results can merit further research, but usually things fall apart on the road to human trials). One 2012 study published by scientists at the University of British Columbia shows that oregano can inhibit flu viruses, but the effect is very weak, and it comes with a nasty side effect: it kills uninfected lung cells. (pdf)

    As for oregano and the microbiome: I’ve only found one published study on this. It seems to inhibit one species that lives in the stomach, H. pylori. Like a number of species, H. pylori is both good and bad for us. It appears to prime our immune system in youth, but in later years it can lead to ulcers and gastric cancer. As is so often the case when it comes to the microbiome, it’s complicated.]

  23. Nice article on a very important subject… what I’ve been calling Endoecology.

    In external ecology we’ve found that in general more diverse ecosystems are more stable and resistant to external influences… perhaps we should all shore up our microflora diversity with “transplants” from various other cultures! A fecal transplant from some rural Mexicans is likely to confer immunity to Montezuma’s revenge, for example.

  24. I enjoyed the article. That said, your comment on errors, [CZ: I do the best I can, Robert. Corrections are always appreciated.] is actually, to me, rather silly. You can do better. It’s simple. One prof I had had a simple rule that any mistakes in spelling or any typos resulted in an F. Period. No if ands or buts. No one had any errors given that motivation (threat).

  25. “CZ: I’m not aware of any research showing antibiotics given to livestock can survive all the way to the dinner table.”

    Feedlot animals are fattened with grain and a constant diet of antibiotics. It seems highly unlikely that given the overload of food and antibiotics that they are immediately metabolized during the fattening process, and more likely that they are still circulating through the body of the animal at the time of slaughter. They are taken directly from the feedlot to slaughter, so there’s no clean out period.

  26. There is also peer reviewed science that indicates a potential link between the use of antibiotics in young children and the subsequent distruption of normal GI flora and autism. (No, no the stupid Jennie McCarthy vaccination and autism pseudo-science nonsense) http://www.sciencedirect.com/science/article/pii/S1075996411002423

    The Canadian Broadcasting Corporation’s Nature of Things had a good special on this topic. Called the Autism Enigma. http://www.cbc.ca/natureofthings/episode/autism-enigma.html

  27. My doctor tole me I had asthma and last winter I suffered repeated chest infections that required antibiotics. After referral to a consultant chest specialist, I underwent numerous tests that showed that I was suffering not from asthma, but from something being produced by my gut. My lungs were 120 percent better than my age prediction. I have been a lifelong swimmer. I had also had a lesion at the corner of my mouth for over a year, that my doctor said was nothing. My dentist, however identified it as thrush, but said it was curious as it was only on the right corner of my mouth and their were no obvious signs or oral infection. He asked which side I slept on and I told him, my right side. He said it is probably coming from your gut, and a light bulb went off in my head. The dentist prescribed topical anti fungal cream, to no effect and my doctor tried a different medicine, but with no effect. I researched on the web and found a low sugar diet that was promoted by a doctor that promised to clear the Candida albicans overgrowth in two months. I tried the diet and gradually the wheezing and chestiness started to subside and eventually cleared altogether. This improvement also coincided with the healing of the lesion that had been intractable for almost two years. I have been free of asthma symptoms ever since and avoid antibiotics. My family has a tendency to type two diabetes and I have wondered since, of imbalances in gut flora that result from high sugar, western diets and the widespread use of antibiotics have resulted in yeast like flora that are capable of suppressing insulin. From the viewpoint of natural selection an organism that feeds on sugars, would have an advantage were it able to manipulate its host to maintain such a high sugar environment. Sorry for the narrative, but someone out there may read this and find something useful.

  28. I’ve seen that this article has been written almost 4 years ago, however I’m still hoping that I’d get a response. It was very interesting however I’m curious about vancomycin in the treatment of infective endocarditis caused by alphahaemolectic streptococcus. When this drug proves futile what is the next course of action? Can a “weaker” drug be used and succeed? And how does the patient recover post treatment… Esp on the onslaught of poor kidney function? Thank you in advance!

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